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High-sensitivity cardiac troponin testing has received much hype over the last decade. Substantial focus on high-sensitivity cardiac troponin testing has occurred due to the combination of diagnostic company marketing, different labelling requirements across regulatory bodies and investigators and journals using different terminology.1 There is a need for agreement on what constitutes a high-sensitivity cardiac troponin assay.1 2 This is not a trivial point, as publications in influential journals still misclassify cardiac troponin assays and their clinical use, despite laboratory recommendations providing some guidance in this area.1 2
So what is a high-sensitivity cardiac troponin assay? The current classification is subjective with the main criterion being that the concentrations are detectable in at least 50% of a healthy population.1 This qualitative approach for classification based on analytical sensitivity has met some resistance; however, it is important to emphasise that this is the first step in developing more rigorous criteria.1 Herein, incorporating clinical utility has the potential to further refine high-sensitivity cardiac troponin assays, and acute coronary syndromes (ACS) represents a crucial setting for refining this test’s characteristics.
Data from prototype assays, to investigational use, to regulatory-approved high-sensitivity cardiac troponin assays in both ACS and secondary prevention populations have demonstrated the ability to identify patients at both low and high risk for long-term cardiovascular outcomes.3–5 In these settings, the risk-stratification ability has been acknowledged, but important gaps remain on how to use high-sensitivity cardiac troponin testing after an ACS diagnosis to aid in patient management and possible treatment for secondary prevention.
In this issue of the Journal, Adamson and colleagues provide important evidence for the measurement of a high-sensitivity cardiac troponin assay months after an ACS diagnosis (ie, 1, 4 and 12 months post ACS).6 In nearly 1800 patients, at 4 months after an …
Contributors PK wrote the manuscript with critical revision from PJD.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests PK has received grants/reagents/consultant/advisor/ honoraria from the laboratory diagnostic industry, specifically from Abbott Laboratories, Beckman Coulter, Ortho Clinical Diagnostics, Randox Laboratories, Roche Diagnostics and Siemens Healthcare Diagnostics. McMaster University has filed patents with PK listed as an inventor in the acute cardiovascular biomarker field. PJD is a member of a research group with a policy of not accepting honorariums or other payments from industry for their own personal financial gain. They do accept honorariums/payments from industry to support research endeavours and costs to participate in meetings. Based on study questions PJD originated and grants he has written, he has received grants from Abbott Diagnostics, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol-Myers-Squibb, Coviden, Octapharma, Philips Healthcare, Roche Diagnostics and Stryker. He has also participated in an advisory board meeting for GlaxoSmithKline and an expert panel meeting with AstraZeneca, Boehringer Ingelheim and Roche.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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